Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microbial -Enzymatic Mucin Metabolic Relay Suppresses Tumor Progression in Apcmin/+ mice

ABSTRACT:

Compelling evidence established the gut microbiota as a pivotal regulator of colorectal cancer (CRC) progression, although stage-specific mechanisms remain unclear. Our investigation in Apcmin/+ mice mapped tumor growth and microbial shifts across early, intermediate, and advanced stages. In Apcmin/+ mice, tumor growth exhibited an initial rapid phase followed by a gradual deceleration. Our study elucidated a niche complementarity model of gut microbiota in suppressing CRC progression: both critical gut bacteria (Akkermansia muciniphila, Muribaculaceae and other taxa) and their enzymes (hexosaminidase and SusD) exhibited the relay pattern in metabolizing intestinal mucin and producing N-acetylglucosamine (GlcNAc). Furthermore, rectal administration of GlcNAc suppressed Wnt/β-catenin signaling activation, might potentially contributing to the deceleration of tumor growth in the mid-to-late stages of cancer. This interplay between gut bacteria may reflect the significance of functional redundancy in maintaining the stability of microbial function.

INSTRUMENT(S): Liquid Chromatography MS - - - Gas Chromatography MS - positive

PROVIDER: MTBLS12770 | MetaboLights | 2025-07-24

REPOSITORIES: MetaboLights

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	a_MTBLS12770_GC-MS_positive__metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS12770_GC-MS_positive__metabolite_profiling_v2_maf.tsv	Tabular
	s_MTBLS12770.txt	Txt

Items per page:

1 - 4 of 4

Similar Datasets

Microbial -Enzymatic Mucin Metabolic Relay Suppresses Tumor Progression in Apcmin/+ mice

Project description:<p>Compelling evidence established the gut microbiota as a pivotal regulator of colorectal cancer (CRC) progression, although stage-specific mechanisms remain unclear. Our investigation in Apcmin/+ mice mapped tumor growth and microbial shifts across early, intermediate, and advanced stages. In Apcmin/+ mice, tumor growth exhibited an initial rapid phase followed by a gradual deceleration. Our study elucidated a niche complementarity model of gut microbiota in suppressing CRC progression: both critical gut bacteria (Akkermansia muciniphila, Muribaculaceae and other taxa) and their enzymes (hexosaminidase and SusD) exhibited the relay pattern in metabolizing intestinal mucin and producing N-acetylglucosamine (GlcNAc). Furthermore, rectal administration of GlcNAc suppressed Wnt/β-catenin signaling activation, might potentially contributing to the deceleration of tumor growth in the mid-to-late stages of cancer. This interplay between gut bacteria may reflect the significance of functional redundancy in maintaining the stability of microbial function.</p>

2025-07-20 | MTBLS12754 | MetaboLights

Global methylation analysis of development and progression of colorectal carcinoma

2016-05-13 | GSE77954 | GEO

Global methylation analysis of development and progression of colorectal carcinoma

Project description:Colorectal tumorigenesis proceedes through well defined clinical stages assoicated with charateristic mutations. Besides genetic alterations, epi-driver genes that are aberrantly expressed in cancers in a fashion that confers a seletive growth advantage can also contribute to tumor evolution. To gain a global view of methylation patterns in normal and maliganant colorectal epithelia, we performed genome-wide DNA methylation analysis on DNAs from 48 fresh frozen CRC samples at different stages of CRC progression. We used IlluminaHumanMethylation450 Beadchip to get a broad view of genome-wide DNA methylationdata during CRC progression and identified significantly differentially methylated genes during CRC progression A total of 48 macro-dissected tissues including normal colon tissue, adenomas, carcinomas and metastases were collected by the Department of Pathology at the University of Virginia under the supervision of an experienced pathologist. DNA was extracted and run on IlluminaHumanMethylation450 Beadchip by Expression Analyisis.

2016-05-13 | E-GEOD-77954 | biostudies-arrayexpress

Intestinal tumor expression data from Apcmin/+ mice gavaged by feces from healthy controls or colorectal cancer patients

Project description:Colorectal cancer (CRC) is closely related to gut dysbiosis. We investigated the effects of imbalanced gut microbiota on the progression of intestinal adenoma in Apcmin/+ mice model using fecal microbiota transplantation (FMT). Administration of feces from CRC patients increased tumor proliferation and decreased apoptosis in tumor cells. Abnormal expression of genes related to Wnt-protein binding and lipid metabolic process was observed.

2019-09-16 | GSE136682 | GEO

Microbial Bile acid metabolite, 3-oxo-LCA, prohibits colorectal cancer progression

Project description:Objective: Bile acids (BAs) not only influence gut microbiome composition but are also metabolized by gut bacteria to form various microbial BAs. Among these, 3-oxo-lithocholic acid (-oxo-LCA) and isoalloLCA have been reported to modulate host immunity, suppress intestinal pathogens, and provide anti-aging benefits. However, their specific effects on intestinal epithelial cells (IECs) and their role in colorectal cancer (CRC) progression remain unclear. Design: To investigate the impact of 3-oxo-LCA on intestinal tumorigenesis, we examined its effects on the growth of mouse and human CRC cell lines (CT26, MC38, HCT116), as well as on primary mouse intestinal organoids and patient-derived CRC organoids (PDCOs). Additionally, we evaluated its role in vivo using APCMin/+ mice and multiple CRC models, including syngeneic CT26 and MC38 models, as well as HCT116 and PDX-derived xenografts in NSG (immunodeficient) mice. Results: Our findings show that 3-oxo-LCA is a potent FXR agonist that restores FXR signaling both in vitro and in vivo. This results in reduced growth of CRC cell lines and suppression of intestinal stem cell (ISC)’s proliferation in both mouse organoids and PDCOs. In APCMin/+ mice, 3-oxo-LCA reduced BA levels, enhanced gut barrier function, decreased tumor burden, and blocked tumor initiation. Furthermore, it significantly inhibited tumor progression in syngeneic and xenograft mouse models and promoted apoptosis within the tumors, enhancing cancer cell death. Conclusion: These results underscore the therapeutic potential of 3-oxo-LCA as a novel FXR agonist for CRC treatment, with its ability to inhibit tumorigenesis and progression by modulating epithelial cell proliferation and inducing apoptosis.

2025-08-14 | GSE294276 | GEO

Indole-3-lactic acid suppresses colorectal cancer via metabolic reprogramming

Project description:Colorectal cancer (CRC) is a common malignant neoplasm influenced by both genetic and environmental factors, and its incidence correlates with the composition of the gut microbiota. Relevant studies have demonstrated that gut microbiota dysbiosis is associated with CRC progression. However, the relationship between CRC tumor proliferation and dysregulation of tryptophan metabolism remains unclear. Our investigation addresses the role and mechanisms of amino acid metabolites in tumor progression based on the dysregulation of tryptophan metabolism in clinical CRC patients. Using metagenomic sequencing and targeted tryptophan metabolomics, our research delineates the aberrant levels of indole-3-lactic acid (ILA) in CRC patients. ILA inhibits glycolysis via the STAT3-HK2 axis and exerts a suppressive effect on CRC independent of the aryl hydrocarbon receptor (AHR). By elucidating the inhibitory role of ILA in CRC and uncovering its underlying mechanisms, our study provides a prospective therapeutic avenue for CRC treatment.

2025-06-04 | GSE271802 | GEO

O-GlcNAc expression levels epigenetically regulate colon cancer tumorigenesis by affecting the cancer stem cell compartment via modulating expression of transcriptional factor MYBL1

Project description:To study the regulation of colorectal adenocarcinoma progression by O-GlcNAc, we have focused on the O-GlcNAc-mediated epigenetic regulation of human colon cancer stem cells (CCSC). Xenograft tumors from colon tumor cells with OGT knockdown grew significantly slower than those formed from control cells, indicating a reduced proliferation of tumor cells due to inhibition of OGT expression. Significant reduction of CCSC population was observed in the tumor cells after OGT knockdown, while tumor cells treated with O-GlcNAcase inhibitor showed an increased CCSC population, indicating that O-GlcNAc levels regulated the CCSC compartment. When grown in suspension, tumor cells with OGT knockdown showed a reduced ability to form tumorspheres, indicating a reduced self-renewal of CCSC due to reduced levels of O-GlcNAc. ChIP-seq experiments using an anti-O-GlcNAc antibody revealed significant chromatin enrichment of O-GlcNAc modified proteins at the promoter of the transcription factor MYBL1, which was also characterized by the presence of H3K27me3. RNA-seq analysis showed an increased expression of MYBL1 in tumor cells with OGT knockdown. Forced overexpression of MYBL1 led to a reduced population of CCSC and tumor growth in vivo, similar to the effects of OGT silencing. Moreover, two CpG islands near the TSS site of MYBL1 were identified, and O-GlcNAc levels regulated their methylation status. These results strongly argue that O-GlcNAc epigenetically regulates MYBL1, functioning similarly to H3K27me3. The aberrant CCSC compartment observed after modulating O-GlcNAc levels, therefore, is likely to result, at least in part, from the epigenetic regulation of MYBL1 expression by O-GlcNAc, thereby significantly affecting tumor progression.

2017-08-25 | GSE93656 | GEO

Transdifferentiation of tumor infiltrating innate lymphoid cells during progression of colorectal cancer

Project description:Innate lymphoid cells (ILCs) reside in mucosal surfaces to potentiate immune responses, sustain mucosal integrity and maintain tissue homeostasis. However, how tumor infiltrating ILCs modulate tumor development and progression is unclear. Here we profiled tumor infiltrating ILCs during colorectal cancer (CRC) progression by single-cell RNA sequencing. We identified six clusters of tumor infiltrating ILCs with unique features. ILC1s expressed inhibitory receptors and underwent inhibitory functional conversion at the late stage of CRC. ILC2s were classified into three subsets (called ILC2-A, -B, -C), ILC2-C subset could facilitate tumor progression. HS3ST1 and PD1 were highly expressed in ILC2s of late stage CRC tumors and deficiency of HS3ST1 or PD1 in ILC2s suppressed tumor growth. Moreover, ILC3s transdifferentiated into ILCregs during CRC progression and ILCregs promoted tumor growth. Of note, TGF- signaling initiated the conversion of ILC3s to ILCregs and blockade of TGF- signaling could disrupt the ILCreg transdifferentiation and inhibited tumor growth as well. Thus intervention of ILC conversions might be a potential strategy for CRC immunotherapy.

2019-12-29 | GSE142694 | GEO

ATF6 promotes colorectal cancer growth and stemness by regulating the Wnt pathway

Project description:The unfolded protein response (UPR) maintains endoplasmic reticulum (ER) homeostasis by sensing protein-folding stress and orchestrating cellular adaptation via the ER-transmembrane proteins IRE1, PERK and ATF6. Malignant cells can co-opt UPR signaling by IRE1 and PERK to sustain tumor growth; however, the importance of ATF6 in cancer remains poorly deciphered. We observed elevated ATF6 transcriptional activity in several cancers including colorectal carcinoma (CRC). Genetic silencing or small molecule inhibition of ATF6 blocked cell cycle progression and reduced viability of several human CRC cell lines in vitro and disrupted tumor progression in vivo. Unexpectedly, ATF6 interference also disabled Myc and Wnt signaling and reduced stemness. ATF6 inhibition attenuated growth of organoids derived from malignant but not normal human intestinal tissue, reducing Wnt-pathway activity and driving cellular differentiation. Wnt-surrogate agonism rescued the growth inhibitory phenotype of ATF6 interference. Our findings identify ATF6 as an unexpected facilitator of oncogenic Wnt signaling in CRC.

2024-08-12 | MSV000095581 | MassIVE

Traditional Chinese Medicine JianPiHuaTan Formula Improving Quality of Life and Survival in Patients with Colorectal Cancer through RAS/RAF Downstream Signaling Pathways

Project description:Abstract Objective: JianPiHuaTan Formula (JPHTF), a traditional Chinese medicine (TCM), has been utilized as an adjunctive therapy for colorectal cancer (CRC). The study aims to evaluate the potential clinical benefits of JPHTF and its effectiveness in inhibiting tumor growth. Methods: 300 stage II/III CRC patients and 412 advanced CRC patients were enrolled to verify the clinical value of JPHTF in CRC treatment. Furthermore, CRC patient-derived xenograft (PDX) mice were utilized to investigate the regulatory mechanisms of JPHTF. Results: JPHTF significantly improved abdominal distension, shortness of breath, drowsiness, loss of appetite, sleep, and tiredness in stage II/III CRC patients, thereby improving their quality of life. Simultaneously, JPHTF served as a supportive therapy in extending the overall survival (OS) of stage IV CRC patients with RAS/RAF mutations undergoing chemotherapy. Additionally, JPHTF effectively impeded tumor progression in CRC PDX models with RAS mutation, accompanied by a reduction in tumor cell content in the JPHTF group. Transcriptomic analysis revealed the involvement of the Hippo and Hedgehog signaling pathways in JPHTF-mediated CRC inhibition. Furthermore, mice in the JPHTF group exhibited increased immune cell infiltration. Conclusions: These findings suggested that JPHTF may inhibits tumor growth in CRC with RAS mutation by modulating RAS/RAF downstream signaling pathways, specifically the Hippo and Hedgehog signaling, leading to increased immune cell infiltration.

2024-06-15 | GSE269502 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data